Diabeticcpg small 2 (Part 5) potx

PATHWAY #5 DIABETIC FOOT DISORDERS VOLUME 45, NUMBER 5, SEPTEMBER/OCTOBER 2006 S–37 S–38 THE JOURNAL OF FOOT & ANKLE SURGERY Figure 12 Diabetic neuroarthropathy, or Charcot foot, is believed to be a neurologically-mediated com- plication of diabetes, with the development modified by musculoskeletal stress. The result is osseous frag- mentation and joint subluxation with often significant morphologic changes in the architecture of the foot. Complications of the Charcot foot include ulceration under areas of bony prominence and potential ampu- tation often related to infection/osteomyelitis that develops adjacent to the area of ulceration. DIABETIC FOOT DISORDERS VOLUME 45, NUMBER 5, SEPTEMBER/OCTOBER 2006 S–39 If the patient presents with a warm, edematous, erythema- tous, insensate foot, plain radiographs are invaluable in ascertaining presence of osteoarthropathy (493, 494). In most cases, no further imaging studies are required to make the correct diagnosis. With a concomitant wound, it may be difficult to differentiate acute Charcot arthropathy from osteomyelitis using plain radiographs alone (133, 183). Additional laboratory studies may prove useful in arriving at a correct diagnosis. The white blood cell count (WBC) with a left shift will often be elevated in acute osteomyelitis, although this can be blunted in diabetic patients (453). While the erythrocyte sedimentation rate and C-reactive protein level may also be elevated in acute infection, they often respond similarly to any inflammatory process and are therefore nonspecific. Bone biopsy, when indicated, is the most specific method for distinguishing osteomyelitis from osteoarthropathy in these circumstances. A biopsy consist- ing of multiple shards of bone and soft tissue embedded in the deep layers of synovium is pathognomonic for neuro- pathic osteoarthropathy (495). Technetium bone scans are generally nonspecific in assisting in the differentiation between osteomyelitis and acute Charcot arthropathy (179, 185). Indium scanning, while more expensive, has been shown to be more specific (179, 193, 496). Additional studies to aid in differentiating osteoarthropathy from osteomyelitis include bone scans uti- lizing Tc HMPAO-labeled white blood cells, MRI, and PET scanning (183, 186, 190, 207). Other serologic markers can be helpful for the diagnosis of acute Charcot osteoarthropathy. A marker for increased osteoclastic activity, 1CPT (carboxyterminal telopeptide of type 1 collagen), has been shown to be elevated but occurs without increased levels of procollagen carboxyterminal propeptide (P1CP), a marker for osteoblastic activity (497- 499). Nonetheless, the most important diagnostic aid in this situation remains a high index of clinical suspicion when a neuropathic patient presents with a swollen or deformed foot (478, 493, 494). Classification of Charcot Arthropathy The most common classification system of Charcot arthropathy—the Eichenholtz classification system—is based on radiographic appearance as well as physiologic stages of the process. It divides the condition into three stages: developmental, coalescent, and reconstructive (495). The developmental stage is characterized by signifi- cant soft tissue swelling, osteochondral fragmentation, or joint dislocation of varying degrees. The coalescent stage is marked by a reduction in soft tissue swelling, bone callus proliferation, and consolidation of fractures. The recon- structive stage is denoted by bony ankylosis and hyper- trophic proliferation. Radiologically, the Eichenholtz system is very descrip- tive and useful, but its practical applicability has limita- tions. In clinical practice, the initial stage is considered active, while the coalescent and reconstructive stages are considered quiescent or reparative. More recently, several authors have proposed an earlier stage 0 that corresponds to the initial inflammatory period following injury but prior to the development of characteristic bony radiographic changes (500-503). This prodromal period might be consid- ered a “Charcot in situ” stage. Diagnosis of the condition during this period, in which no deformity has yet devel- oped, could ostensibly arrest further progression of the destructive inflammatory process (494). Another popular classification system is based on five anatomic sites of involvement but does not describe disease activity (129, 136) (Fig 13). Several other classification schemes are described in the literature, but none has been found to be superior or predictive of outcome (500, 504- 506). Management of Acute Charcot Neuroarthropathy Immobilization and stress reduction are the mainstays of treatment for acute Charcot arthropathy (129, 131, 135, 136, 478, 507, 508). Many clinicians advocate complete non-weightbearing through the use of crutches or other assistive modalities during the initial acute period. While this is an accepted form of treatment, three-point gait may in fact increase pressure to the contralateral limb, thereby predisposing it to repetitive stress and ulceration or neuro- pathic fracture (509). A short leg plaster or fiberglass non- weightbearing cast can additionally be used for acute Charcot events, even in patients with noninfected ulcera- tions (129, 135, 481). A soft compressive dressing in con- cert with a removable cast walker or pneumatic walking brace can also be used effectively in this regard (136, 139). Some centers prefer to initially apply a weightbearing total contact cast in the management of acute osteoarthropathy (135, 140, 493, 510-512). These ambulatory total contact casts should be changed at least every 1 to 2 weeks to adjust to limb volume changes as the edema decreases. Following the initial period of off-loading, reductions in skin temperature and edema indicate the stage of quies- cence, at which point the patient progresses into the posta- cute phase of treatment. Progression to protected weight- bearing is permitted, usually with the aid of an assistive device. Through the use of appropriately applied total con- tact casts or other off-loading modalities (eg, fixed ankle walker, bivalved casts, total contact prosthetic walkers, S–40 THE JOURNAL OF FOOT & ANKLE SURGERY patellar tendon-bearing braces), most patients may safely ambulate while bony consolidation of fractures progresses (129, 135, 477, 478). Charcot restraint orthotic walkers (CROW) or other similar total contact prosthetic walkers have gained acceptance as useful protective modalities for the initial period of weightbearing (513-515). A more read- ily available option is a pneumatic walking brace or similar removable cast walker that might incorporate a cushioned foot bed or insole. These “instant total contact casts” are made nonremovable by simply applying tape or a fiberglass cast roll around the body of the walker to help encourage compliance (50, 516). The mean time of rest and immobilization (casting fol- lowed by removable cast walker) prior to return to perma- nent footwear is approximately 4 to 6 months (133-135, 474, 478, 493). Custom full-length inserts and comfort or Figure 13 Diabetic neuroarthropathy may be classified according to the anatomic location of joint involvement. The relative percentage of frequency of involvement is given. (Adapted from Sanders LJ and Frykberg RG. The High Risk Foot in Diabetes Mellitus, p108, Churchill Livingstone, New York, 1991) extra-depth shoes should be worn when protective bracing is no longer required (136, 138, 513). Moderately unstable ankles will benefit from an ankle foot orthosis (AFO) and high-top therapeutic shoe, while a severely unstable or maligned rearfoot will require a patellar tendon-bearing (PTB) brace incorporated into a custom shoe (493, 517, 518). The PTB brace has reportedly decreased mean rear- foot peak forces by at least 32% (517). There is recent interest in the adjunctive use of bisphos- phonate therapy in acute Charcot arthropathy to help expe- dite conversion of the acute process to the quiescent, repar- ative stage (519-521). These pyrophosphate analogs are potent inhibitors of osteoclastic bone resorption and are widely used in the treatment of osteoporosis, Paget’s dis- ease, and reflex sympathetic dystrophy syndrome (50, 130). One randomized trial in the UK compared the use of a sin- DIABETIC FOOT DISORDERS VOLUME 45, NUMBER 5, SEPTEMBER/OCTOBER 2006 S–41 gle intravenous infusion of pamidronate with the use of saline infusion (498). The treatment group had significant declines in temperature and bone turnover markers (deoxypyridinoline crosslinks and bone specific alkaline phosphatase) in subsequent weeks compared with the con- trol group, but no differences in clinical or radiographic out- comes were reported. A small trial comparing 6 months of oral alendronate plus off-loading with standard off-loading alone in acute Charcot patients found that the study group had significant reductions in 1CTP and hydroxyprolin, both of which are markers of bone resorption and increased foot bone density (499); no differences in clinical outcomes were noted. Similarly, electrical bone growth stimulation has been applied to the management of acute neuroarthropathy to promote rapid consolidation of fractures (522-524). Low- intensity pulsed ultrasound (LIPUS) has also been suggest- ed as a useful adjunct in promoting healing of Charcot frac- tures (525). Although promising in theory, none of these adjunctive treatments have yet been conclusively proven effective through large prospective multicenter, randomized trials. Surgical Management of Charcot Osteoarthropathy Reconstructive surgery in acute Charcot may be consid- ered if a deformity or instability exists that cannot effec- tively be controlled or accommodated by immobilization and off-loading (136, 140, 478, 500, 510, 511, 526). If the neuroarthropathy is identified in its early stages and non- weightbearing is instituted, surgery is usually unnecessary. According to consensus opinion, surgery in the acute stage is generally nonadvisable due to the extreme hyperemia, osteopenia, and edema present (131, 132, 134, 135, 477, 511, 527, 528). However, surgical intervention during the acute phase may be considered in the presence of acute subluxation without osteochondral fragmentation (509, 529). One small series reported successful arthrodeses rates with preserved foot function in patients with acute arthropathy of the midfoot (530). Nevertheless, this aggressive surgical approach needs confirmation through larger comparative trials prior to its adoption in the routine management of the acute Charcot foot. As few as 4% to as many as 51% of patients presenting to tertiary centers are reported to undergo surgical procedures for Charcot deformities (474, 527, 528). However, such centers often receive chronic cases from multiple referral Figure 14 Severe midfoot collapse due to Charcot neuroarthropathy as shown (A) on radiograph and (B) in clinical presentation. (C) This patient was treated with tarsometatarsal arthrodesis using a multiplanar circular external fixator. (D) A postoperative radiograph and (E) clinical photograph at 4 months postoperative are shown here. sources and with various degrees of deformity present; therefore, their rate of operation on these patients does not reflect the true incidence or need for such treatment in the community. A recent review of one center’s experience with midfoot neuroarthropathy in 198 patients (201 feet) indicated that more than half of these patients could be suc- cessfully managed without surgery (510). Hence, large pop- ulation-based studies are needed to assess the need for sur- gical intervention and compare the efficacy of various con- servative therapies (474, 493, 520). The goal of any surgery on the acute or chronic Charcot foot is to create a stable, plantigrade foot that may be appro- priately accommodated (140, 478, 510, 530, 531). Most S–42 THE JOURNAL OF FOOT & ANKLE SURGERY operations on chronic Charcot feet consist of exostectomies for prominent plantar (‘rocker-bottom”) deformities caus- ing ulceration when the remainder of the foot is stable (135, 505, 511, 532) (Fig 14). However, more complex arthrodesis procedures are performed with increasing fre- quency and success, often using circular external fixation or intramedullary nails (140, 478, 526, 531, 533-537). These include isolated or multiple midfoot (Fig 15) or hindfoot fusions, triple arthrodeses, tibiocalcaneal fusions (Fig 16), and ankle fusions (538-542). Following surgery, patients are immobilized until skin temperatures and postoperative edema normalize. As with patients treated nonsurgically, after prolonged cast immobi- Figure 15 (A) This Charcot patient presented with a recalcitrant ulceration below an area of bony prominence, (B) as shown on radiograph. Surgical management consisted of exci- sion of the ulcer, (C) exostectomy, and (D) primary wound closure. DIABETIC FOOT DISORDERS VOLUME 45, NUMBER 5, SEPTEMBER/OCTOBER 2006 S–43 Figure 16 This neuropathic diabetic patient sustained an ankle fracture and underwent open reduction internal fixation. (A) At 3 months postoperatively, radiographs revealed Charcot disor- ganization and loss of reduction. (B) The patient was brought back to surgery for talectomy and tibiocalcaneal fusion, shown in this intraoperative image. (C) A multiplanar circular external fixator was applied to accomplish the arthrodesis procedure. (D) Radiograph shows union at the arthrodesis site at 5 months postoperative. . consolidation of fractures ( 522 - 524 ). Low- intensity pulsed ultrasound (LIPUS) has also been suggest- ed as a useful adjunct in promoting healing of Charcot frac- tures ( 525 ). Although promising in. 1 32, 134, 135, 477, 511, 527 , 528 ). However, surgical intervention during the acute phase may be considered in the presence of acute subluxation without osteochondral fragmentation (509, 529 ) management of acute osteoarthropathy (135, 140, 493, 510-5 12) . These ambulatory total contact casts should be changed at least every 1 to 2 weeks to adjust to limb volume changes as the edema decreases. Following